N-Acetyl-chitobiose ameliorates metabolism dysfunction through Erk/p38 MAPK and histone H3 phosphorylation in type 2 diabetes mice

• Published in: Journal of functional foods 2017-01, Vol.28, p.96-105
• Main Authors: Wu, Xia, Wang, Jing, Shi, Yuqin, Chen, Sai, Yan, Qiaojuan, Jiang, Zhengqiang, Jing, Hao
• Format: Article
• Language: English
• Subjects: Histone H3; Insulin resistance; Mitogen-activated protein kinase; N-Acetyl chitobiose; Type 2 diabetes
• ISSN: 1756-4646; 2214-9414
• DOI: 10.1016/j.jff.2016.11.012

•This is the first study on the improvement of N-acetyl-chitobiose on diabetes-related metabolism disorders.•N-Acetyl-chitobiose lowered blood glucose and improved glucose intolerance and insulin sensitivity.•N-Acetyl-chitobiose inhibited MAPK signaling pathways in type 2 diabetes model mice. The effects of N-acetyl-chitobiose [(GlcNAc)2] on diabetes-related metabolic disorders, along with its regulation mechanism of mitogen-activated protein kinase (MAPK) signaling pathway were investigated on type 2 diabetes (T2D) model mice. Treatment with (GlcNAc)2 improved significantly glucose and lipid metabolism by decrease of blood glucose (∼20%), total cholesterol (∼26.5%) and triglyceride (∼16.1%), increase of HDL-cholesterol (∼107.2%), and reversal of insulin resistance in T2D model mice. Moreover, (GlcNAc)2 reduced lipid peroxidation and inflammatory factors in pancreas with increased activity of superoxide dismutase (∼57%), reduced malondialdehyde equivalent (∼22%) and lowered levels of TNF-α, IL-1β and NF-κB. (GlcNAc)2 had also significantly attenuated MAPK signaling pathways especially though IL-1β-Erk/p38-Histone H3 pathway in T2D model mice. It can be concluded that (GlcNAc)2 has potential as a new functional food ingredient to improve T2D-related metabolic disorders.